The gut microbiome molecular mimicry piece in the multiple sclerosis puzzle

被引:16
作者
Elsayed, Noha S. S. [1 ]
Aston, Paula [2 ]
Bayanagari, Vishnu R. R. [1 ]
Shukla, Sanjay K. K. [1 ]
机构
[1] Marshfield Clin Res Inst, Ctr Precis Med Res, Marshfield, WI 54449 USA
[2] Marshfield Clin Hlth Syst, Dept Neurol, Marshfield, WI USA
关键词
multiple sclerosis; gut microbiome; molecular mimicry; microbial metabolites; aberrant immune response; leaky gut; HLA genes; Epstein-Barr virus; CHAIN FATTY-ACIDS; CD4(+) T-CELLS; DISEASE COURSE; GENETIC RISK; BACTERIA; IMMUNE; SUSCEPTIBILITY; RECEPTOR; PEPTIDOGLYCAN; INFLAMMATION;
D O I
10.3389/fimmu.2022.972160
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The etiological complexity of multiple sclerosis, an immune-mediated, neurodegenerative disease with multifactorial etiology is still elusive because of an incomplete understanding of the complex synergy between contributing factors such as genetic susceptibility and aberrant immune response. Recently, the disease phenotypes have also been shown to be associated with dysbiosis of the gut microbiome, a dynamic reservoir of billions of microbes, their proteins and metabolites capable of mimicring the autoantigens. Microbial factors could potentially trigger the neuroinflammation and symptoms of MS. In this perspective article, we discussed how microbial molecules resulting from a leaky gut might mimic a host's autoantigen, potentially contributing to the disease disequilibrium. It further highlights the importance of targeting the gut microbiome for alternate therapeutic options for the treatment of MS.
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页数:10
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